Gram-negative Bacteria Infections in Healthcare SettingsOn this PageGeneral Information about gram-negative bacteriaCDC guidelines to address gram-negative bacteriaOutbreak investigationsLaboratory tests for detecting resistanceMonitoring gram-negative healthcare-associated infectionsGeneral Information about gram-negative bacteriaGram-negative bacteria cause infections including pneumonia, bloodstream infections, wound or surgical site infections, and meningitis in healthcare settings. Gram-negative bacteria are resistant to multiple drugs and are increasingly resistant to most available antibiotics. These bacteria have built-in abilities to find new ways to be resistant and can pass along genetic materials that allow other bacteria to become drug-resistant as well. CDC’s aggressive recommendations, if implemented, can prevent the spread of gram-negatives.Gram-negative infections include those caused by Klebsiella, Acinetobacter, Pseudomonas aeruginosa, and E. coli., as well as many other less common bacteria. Top of PageCDC guidelines to address gram-negative bacteria CDC Multi-Drug Resistant Organism Guidelines address reducing infections caused by all drug-resistant bacteria, including gram negatives.CDC Guidance for Control of Infections with Carbapenem-resistant or Carbapenemase-producing Enterobacteriaceae in Acute Care Facilities contains specific recommendations for prevention and control of a specific emerging drug-resistant gram-negative.Top of PageOutbreak investigationsOutbreak investigations have led to a better understanding of how to control these bacteria in healthcare. In the past 3 years, the Division of Healthcare Quality Promotion has assisted in at least 10 investigations of outbreaks of gram negative infections. CDC has collaborated with state health departments in Maryland and Arizona to successfully control outbreaks of Multidrug-resistant-Acinetobacterinfections occurring among intensive care unit patients.CDC has worked with the Puerto Rico health department to control an outbreak of highly resistant Klebsiella at a neonatal intensive-care unit in Puerto Rico.CDC assisted the Ohio health department’s investigation of infections caused by Acinetobacter. These outbreaks have occurred in various healthcare facilities in the state of Ohio and have been controlled by aggressive infection control interventions.CDC worked with the state health department of Texas on separate outbreaks of B. cepacia and Pseudomonas. Additionally, CDC worked with the state health department in Georgia on an unrelated outbreak of B. cepacia. CDC worked with the Department of Defense to investigate and control Acinetobacterinfections occurring in soldiers injured in the Middle East. This collaboration led to important improvements in infection control in military medical facilities. In addition to these outbreaks, CDC’s reference laboratory has confirmed carbapenemase resistance in bacteria for 32 other U.S. states.Top of PageLaboratory tests for detecting resistance CDC is collaborating with laboratory standards-setting institutions to identify and recommend laboratory tests for the accurate detection of carbapenemase-mediated resistance. CDC is working with states to identify isolates with unusual resistance and to determine new mechanisms of resistance among multidrug-resistant gram-negatives, including the recent identification of a new mechanism of resistance in patients returning from Asia.Gram negative bacteria (Pseudomonas aeruginosa) are simply called so because of their detection by the Gram staining test in which they do not retain the crystal violet color (dye) in their cell wall. The bacterial cell wall holds the pink or reddish dye once a counterstain chemical is used.Cell Wall StructureThe outer layer of Gram negative bacterial cell wall is made up of lipopolysaccharide and protein (core and O-polysaccharide and lipid A) and it covers a very few thinner layers of peptidoglycan as compared to Gram positive bacteria (peptidoglycan forms the outer layer of the Gram positive bacterial cell wall) and does not contain lipoproteins. The outer layer of the cell wall contains porins (pore-like structure for a specific type of molecule). Below the outer layer of lipopolysaccharide, there exist layers of periplasmic space (space between two layers of peptidoglycan and internal cell membrane) and plasma membrane. Some of these negative bacteria also have flagella with four surrounding rings.The cell wall also home a component that helps in endotoxic activity and it also has pyrogenic effects associated with the Gram negative infections. The bacterial side wall also has a part which is called side chain that is made up of lipopolysaccharide (and has hexoses in various chemical compositions as a part of its structures). These side chains carry bases of somatic antigen. These side chains are very important in order to classify the Gram negative bacteria based on their chemical composition.
Characteristics of Gram Positive BacteriaThese bacteria are encapsulated by a bilipid layer. The outer membrane of the Gram-negative bacteria is absent in the Gram-positive ones. Some of the species of these bacteria possess flagella for locomotion. The examples of Gram-positive bacteria and their description are presented below.
As Mycobacterium are unable to be visualised on standard haematoxylin and eosin (H+E) and gram stains, the ZN stain was developed. It is based on the tubercle bacilli having a lipid-rich cell wall that takes up phenol-dye solutions (eg. carbolfuchsin, the main dye used in the ZN stain) and after subsequent differentiation, retains the phenol-dye.SolutionsCarbolfuchsin – (1g basic fuchsin in 10ml ethanol) + (5g phenol in 100ml distilled water), then filter.Methylene Blue – 0.2% methylene blueMethod1. Take sections to water.2. Cover section with filtered carbolfuchsin for 20 minutes.3. Wash well in tap water.4. Differentiate in 1% acid alcohol until section is a very pale pink.5. Wash well in tap water.6. Stain with methylene blue for 1 minute.7. Dehydrate, clear and mount.
Silver staining is used to detect proteins after electrophoretic separation on polyacrylamide gels. It combines excellent sensitivity (in the low nanogram range) whilst using very simple and cheap equipment and chemicals. It is compatible with downstream processing such as mass spectrometry analysis after protein digestion. The sequential phases of silver staining are protein fixation, then sensitization, then silver impregnation and finally image development. Several variants of silver staining are described here, which can be completed in a time range from 2 hours to one day after the end of the electrophoretic separation. Once completed, the stain is stable for several weeksMaterials Needed:Silver Nitrate 1% Citric Acid: 100 ml of DI water + 1 g of Citric Acid 30 % NaOH(7.5 M): 100 ml of DI water + 30 g of NaOH14.8 M Ammonium Hydroxide 38% Formaldehyde Ultra-pure water, use this for all steps and reagents 50% Aqueous Glutaraldehyde (optional) Glass tray or Novex Stain Ease Gel tray. If using glass, make sure to clean well with soap and DI water. If using Novex tray, use only trays designated for use with silver staining – do not use trays which have been used for coomassie staining Method:Make 7% Acetic Acid: 186 ml of water + 14 ml of acetic acid Make 50% Methanol: 200 ml of water + 200 ml of methanol. Optional – for extra fixation/crosslinking add 240 µl of 50% glutaraldehyde to the 50% methanol (makes solution 0.03% glutaraldehyde). Soak gel in 7% acetic acid for 7 minutes. Soak gel in 200 ml of 50% methanol for 20 minutes. Soak gel in 200 ml of 50% methanol for 20 minutes. Prepare Solution A: 0.8 g of silver nitrate + 4 ml of water Rinse gel in ~200 ml water for 10 minutes Rinse gel in ~200 ml water for 10 minutes Note: Steps 7 and 8 are very important for the NuPAGE gels if you skip these steps or do not rinse the gel for long enough the gel will develop too quickly and have significantly more background.5 minutes before end of final water rinse prepare solution B: 21 ml of water + 250 ul of 30% NaOH (to make 0.36%) + 1.4 ml of 14.8M ammonium hydroxide To make staining solution: add solution A to solution B dropwise while stirring then add 76 ml of water. Soak gel in the staining solution for 15 minutes Rinse gel in ~200 ml water for 5 minutes Rinse gel in ~200 ml water for 5 minutes Make developing solution: 200 ml of water + 1 ml of 1% citric acid + 100 ul of 37% formaldehyde Soak gel in developing solution until bands are visible usually 2 to 15 minutes Stop development by rinsing gel with 3 changes of ~200 ml water The sensitivity of this method should be in the 10ng/band range.Silver Stains Silver staining is the most sensitive colorimetric method for detecting total protein. The technique involves the deposition of metallic silver onto the surface of a gel at the location of protein bands. Silver ions (from silver nitrate in the stain reagent) interact and bind with certain protein functional groups. Strongest interactions occur with carboxylic acid groups ( Asp and Glu), imidazole (His), sulfhydryls (Cys), and amines (Lys). Various sensitizer and enhancer reagents are essential for controlling the specificity and efficiency of silver-ion binding to proteins and effective conversion (development) of the bound silver to metallic silver. The development process is essentially the same as for photographic film; silver ions are reduced to metallic silver, resulting in brown-black color.Silver staining protocols require several steps that are affected by reagent quality as well a incubation times and thickness of the gel. An advantage of commercially available silver staining kits is that the formulations and protocols are optimized and consistently-manufactured, helping to minimize the effects of minor differences in day-to-day use. Kits with optimized protocols are robust and easy to use, detecting less than 0.5 nanograms of protein in typical gels.Silver stains use either glutaraldehyde or formaldehyde as the enhancer. These reagents can cause chemical crosslinking of the proteins in the gel matrix, limiting compatible with destaining and elution methods for analysis by mass spectrometry (MS). Therefore, optimization of sensitivity vs. protein-recoverability is critical when silver staining as part of an MS-workflow.Silver stain formulations can be made such that protein bands stain black, blue-brown, red or yellow, depending on their charge and other characteristics. This is particularly useful for differentiating overlapping spots on 2D gels.
Description: This method is used for detection of glycogen in tissues such as liver, cardiac and skeletal muscle on formalin-fixed, paraffin-embedded tissue sections, and may be used for frozen sections as well. The glycogen, mucin, and fungi will be stained purple and the nuclei will be stained blue. Fixation: 10% formalin. Section: paraffin sections at 5 um. Solutions and Reagents: 0.5% Periodic Acid Solution: Periodic acid ---------------------- 0.5 g Distilled water -------------------- 100 ml Schiff Reagent: Test for Schiff reagent: Pour 10 ml of 37% formalin into a watch glass. To this add a few drops of the Schiff reagent to be tested. A good Schiff reagent will rapidly turn a red-purple color. A deteriorating schiff reagent will give a delayed reaction and the color produced will be a deep blue-purple. Mayer’s Hematoxylin Solution: Procedure: 1. Deparaffinize and hydrate to water. 2. Oxidize in 0.5% periodic acid solution for 5 minutes. 3. Rinse in distilled water. 4. Place in Schiff reagent for 15 minutes (Sections become light pink color during this step). 5. Wash in lukewarm tap water for 5 minutes (Immediately sections turn dark pink color). 6. Counterstain in Mayer's hematoxylin for 1 minute.7. Wash in tap water for 5 minutes. 8. Dehydrate and coverslip using a synthetic mounting medium. Results: Glycogen, mucin and some basement membranes --- red/purple Fungi ------------------------------------------------------ red/purple Background ----------------------------------------------- blue PAS Staining Kit is used to demonstrate the presence of glycogen in tissue. PAS-positive reticular fibers, basement membrane, fungus, and neutral mucopolysaccharides are also detected. PAS Staining Kit may also be used to aid in distinguishing a PAS-positive, secreting adenocarcinoma from undifferentiated PAS-negative squamous cell carcinoma. PAS Staining Kit uses Periodic Acid to oxidize glycols to aldehydes. Schiff's Reagent forms a colorless dialdehyde compound that is transformed to the colored final staining of glycol-containing cellular components. PAS staining in tissue sections and digestion with diastase is useful as an aid in the diagnosis of glycogen storage disease. The PAS Staining Kit stains glycogen bright magenta, with cell nuclei staining light purple.
The stain may also be used as an aid in the identification of Cryptococcus neoformans, a pathogenic fungus containing mucin in its capsule.
The use of Giemsa stain is the most reliable procedure to stain malaria blood film, which is composed of eosin and methylene blue. The eosin component stains the parasite nucleus red, while the methylene component stains the cytoplasm blue. Proper preparation of Giemsa staining of high quality standardized malaria blood thick and thin films on the glass slides to be used in microscopy centers must be observed.a. Ensure that the following materials, reagents and supplies are available for proper preparation of stain:GiemsaStock solution Buffered water (ph 7.2) Methanol Pasteur pipettes Graduated cylinder Drying Rack Staining trough Clean tap water Timing clock b. There are two methods of staining with Giemsa stains: (i) the Rapid (10%) method, and (ii) routine or regular (3%) method; b.1.1 Preparation of 10% Giemsa working solution( mass staining)i. Pour 90 mL of buffered water (ph 7.2) into a 100 mL graduated cylinder;ii. Using a pasteur pipette, draw 10 mL of Giemsa stock solution. Add the stain to the buffered water in the graduated cylinder;iii. Cover the top of the graduated cylinder with parafilm. Gently invert the cylinder several times until completely mixed;iv. Giemsa working solution stain must be discarded through the sink after 24 hours and prepare a fresh working solution again. b.1.2 Preparation of 10% Giemsa working solution (individual slide staining)i. For individual slide staining, each slide needs approximately 3 mL of Giemsa working solution to cover it;ii. Using a Pasteur pipette add 9 drops of Giemsa stock solution to 3ml of buffered water in a 10 mL graduated cylinder. b.1.3 Procedure of Rapid staining of Malaria blood filmsi. Allow thick film to dry completely. If rapid results are required, drying maybe hastened by using a blow drier or briefly exposing the slide to gentle heat such as from the microscope lamp. Care should be taken to avoid overheating, otherwise the thick film will be heat-fixed;ii. Fix the thin film by dipping it briefly in a container with methanol for a few seconds. To permit dehemoglobinization, the thick film should not be fixed; thus avoid methanol or its fumes touch the thick film;iii. Gently pour the stain on the slide using a pipette on the staining assembly. Alternatively, slides can be placed faced down on a concave staining plate and the stain introduced underneath the slide; (not routinely practice);iv. Staining Time: It depends on the age of the Giemsa stock solution. It may extend up to 15 minutes if Giemsa stock is freshly prepared;v. Gently flush the stain off the slide with a clean tap water; do not tip off the stain on the slide and wash, as this will leave a deposit of scum over the smear;vi. Place the slide on the drying rack, film side downwards, to drain and dry making sure that the film does not touch the edge of the rack. b.2 Regular Staining Method (3% Giemsa stain working solution)This regular method is used for staining larger number of slides such as those collected during surveys or research studies. b.2.1 Preparation of 3% Giemsa working solution i. Pour 97 mL of buffered water (ph 7.2) into a 100 mL graduated cylinder; ii. Using Pasteur pipette, draw 3 mL of Giemsa stain. Add the stain to the buffered water in the graduated cylinder; iii. Cover the top of the graduated cylinder with parafilm or gently invert the cylinder several times until completely mixed; iv. Label the cylinder with contents, date and time prepared and technician’s initial; v. Buffered Giemsa stain must be prepared fresh and discarded after 6 hours. b.2.2 Procedure of Regular Staining of Malaria Blood Film i. Fix thin film by briefly dipping it in a container with methanol for a few seconds. Prolong fixation make it difficult to demonstrate Schuffner’s dots and Maurer’s spots. To permit dehaemoglobinization, the thick film should not be fixed, therefore avoid methanol or its vapor touching the film. ii. Place malaria blood film in a staining rack and stain singly, or in batches in staining jar to avoid cross-contamination. Batch staining is advisable only when several malaria blood films are from a single patient. iii. Stain films for 30-45 minutes out of the sunlight. iv. Pour clean tap water gently into the trough to float off the iridescent scum on the surface of the stain. Alternatively, gently immerse the whole trough in a vessel filled with clean tap water. v. Rinse slides briefly and gently under running tap water or by a gentle flow of clean water from a beaker. vi. Place the stained slides in a drying rack to drain and dry, film side downwards, making sure the film does not touch the slide rack. vii. At all times during preparation and storage, slides should be protected from exposure to dust and insects.c. Evaluation of Stained Blood Film c.1 Evaluation of a well-stained blood thin film:i. The background should be clean and free from debris; the color of erythrocyte is a pale grayish pink;ii. Leukocytes have deep purple nuclei and well defined granules;iii. The chromatin of malaria parasite is a deep purplish red and clear purplish blue cytoplasm;iv. Stippling should show up as schuffner’s dots in erythrocytes containing P. vivax or P. ovale, and Maurer’s spots in erythrocytes containing the larger ring forms of P. falciparum. c.2 Evaluation of a well-stained thick film:i. The background should be clean and free from debris, with a pale mottled-grey color derived from the lysed erythrocytes;ii. Leukocytes nuclei are a deep-rich purple;iii. Malaria parasites are well defined with deep-red chromatin pale purplish blue cytoplasm. In P. vivax and P. ovale infections, the presence of schuffner’s stippling in the “ghost” of host erythrocytes can be seen especially at the edge of the film. c.3 Staining quality:i. A malaria blood film that is too pinkish suggests low ph or overstraining;ii. A malaria blood film that is too bluish or purplish suggests high ph, film is too thick or under-stained.
Category ADefinitionThe U.S. public health system and primary healthcare providers must be prepared to address various biological agents, including pathogens that are rarely seen in the United States. High-priority agents include organisms that pose a risk to national security because theycan be easily disseminated or transmitted from person to person;result in high mortality rates and have the potential for major public health impact;might cause public panic and social disruption; andrequire special action for public health preparedness.Agents/DiseasesAnthrax (Bacillus anthracis)Botulism (Clostridium botulinum toxin) Plague (Yersiniapestis) Smallpox (variola major) Tularemia (Francisellatularensis) Viral hemorrhagic fevers (filoviruses [e.g., Ebola, Marburg] and arenaviruses [e.g., Lassa, Machupo])
Suppurative Inflammation — Document Transcript1. Purulent inflammation: Inflammation resulting in large amount of pus, which consists of neutrophils, dead cells, and fluid. Infection by pyogenic bacteria such as staphylococci is characteristic of this kind of inflammation. Large, localised collections of pus enclosed by surrounding tissues are called abscesses. The pus which is the end product of this type of inflammation a whitish-yellow, yellow or yellow-brown exudate produced by vertebrates during inflammatory pyogenic bacterial infections. An accumulation of pus in an enclosed tissue space is known as an abscess, while a visible collection of pus within or beneath the epidermis is known as a pustule or pimple. Pus is produced from the dead and living cells which travel into the intercellular spaces around the affected cells. Examples for this type of inflammation: 1) Suppurative appendicitis 2) Suppurativeotitis 3) Post streptococcal glomerulonephritis 4) Pyelonephritis 5) Brain abscess 6) Purulent meningitis 7) Suppurative lymphadenitis 2. 1) Suppurative appendicitis Appendicitis is a condition characterized by inflammation of the appendix. It is a medical emergency. All cases require removal of the inflamed appendix. Signs and symptoms of acute appendicitis can be classified into two types, typical and atypical. The typical history includes pain starting centrally (periumbilical) before localizing to the right iliac fossa (the lower right side of the abdomen); On the basis of experimental evidence, acute appendicitis seems to be the end result of a primary obstruction of the appendix lumen. Once this obstruction occurs the appendix subsequently becomes filled with mucus and swells, increasing pressures within the lumen and the walls of the appendix, resulting in thrombosis and occlusion of the small vessels, and stasis of lymphatic flow. Rarely, spontaneous recovery can occur at this point. As the former progresses, the appendix becomes ischemic and then necrotic. As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). The end result of this cascade is appendiceal rupture (a 'burst appendix') causing peritonitis, which may lead to septicemia and eventually death. Diagnosis is based on patient history (symptoms) and physical examination backed by an elevation of neutrophilic white blood cells. Atypical histories often require imaging with ultrasound and/or CT scanning. A pregnancy test is vital in all women of child bearing age, as ectopic pregnancies and appendicitis present with similar symptoms. The consequences of missing an ectopic pregnancy are serious, and potentially life threatening. Furthermore the general principles of approaching abdominal pain in women (in so much that it is different from the approach in men) Gross picture: 3. An exemplary case of acute appendicitis in a 10-year-old boy. The organ is enlarged and sausage-like (botuliform). This longitudinal section shows red inflamed mucosa with an irregular luminal surface. Diagnosed and removed early in the course of the disease, this appendix does not show late complications, like transmural necrosis, perforation, and abscess formation. Microscopic picture: A. Brief Descriptions،G4. 1. Cause : It is associated with obstruction (fecalith, gallstone, tumor or ball of worms). 2. Abscess formation within the wall and foci of suppurative necrosis in the mucosa. B. Gross Findings،G 1. Congested & swollen. 2. Dilated lumen contain pus, or a fecalith, or both. 3. Serosa coated with fibrin, fibrinopurulentexudate, or pus. C. Micro Findings،G 1. Mucosal ulceration & infiltration by PMNs, eosinophils, plasma cells, &lymphocytes throughout all layers & frequently into serosa. 2. More advanced stage, the inflammatory process involved the full thickness of wall,with partial necrosis or infarction of wall (perforated areas). D. Others: 1. Classified into acute, suppurative, & gangrenous stages. site acute suppurative gangrenous mucosa neutrophilssuppurative hemorrhagic necrosis ulceration wall neutrophilssuppurative green-black necrosis necrosisserosa congested blood purulent green-black vessels exudates necrosis fibrinous exudates E. Reference،G 1. Robbins Pathologic Basis of Disease, 6th ed. P.839-840. ،@ 2) Pyelonephritis is an ascending urinary tract infection that has reached the pyelum (pelvis) of the kidney. If the infection is severe, the term "urosepsis" is used interchangeably (sepsis being a systemic inflammatory response syndrome due to infection). It requires 5. antibiotics as therapy, and treatment of any underlying causes to prevent recurrence. It is a form of nephritis. It can also be called pyelitis. Acute pyelonephritis is an exudative purulent localized inflammation of the renal pelvis (collecting system) and kidney. The renal parenchyma presents in the interstitium abscesses (suppurative necrosis), consisting in purulent exudate: neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, glomeruli and vessels are normal. Gross pathology often reveals pathognomonic radiations of hemorrhage and suppuration through the renal pelvis to the renal cortex. Chronic infections can result in fibrosis and scarring. Causes: Most cases of "community-acquired" pyelonephritis are due to bowel organisms that enter the urinary tract. Common organisms are E. coli (70-80%) and Enterococcusfaecalis. Hospital-acquired infections may be due to coliforms and enterococci, as well as other organisms uncommon in the community (e.g. Klebsiella spp., Pseudomonas aeruginosa). Most cases of pyelonephritis start off as lower urinary tract infections, mainly cystitis and prostatitis. Untreated infection may spread and leads to gram negative septicemia with shock. In severe infection: - Renal papillary necrosis caused by inflammatory thrombosis of vasa recta supplying the papillae. Perinephric abscess - Infection spreads to perinepheric fat. - Pyonephrosis (Distension of pelvicalyceal system with pus) maybe present. 6. Acute pyelonephritis is an exudative purulent localized inflammation of kidney and renal pelvis. The renal parenchyma presents in the interstitium abscesses (suppurative necrosis), consisting in purulent exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, glomeruli and vessels are normal. (Hematoxylin- eosine, ob. x10) Purulent meningitis Infectious disease that involves the inflammation of the meninges, which often extends to the brain and ventricles, causing ventriculitis. 7. Etiology: Bacteria, fungi, rarely parasites, clinical Headache, stiff neck or back.
Granulomatous InflammationCORE DIFFERENTIAL:1. Foreign body (need to polarize)2. TB, Fungal, Others (Schistosomisasis, Leprosy)3. Sarcoidosis4. Neoplasia5. Collagen vascular diseasesSKINLeprosySyphyllisPalisadinggranulomas:-granulomaannulare-necrobiosislipoidica-rheumatoid noduleTumors:-xanthelasma-Langerhans cell histiocytosis-lymphomaLUNG-TB, fungus, many more…GUKIDNEYMalakoplakiaXanthogranulomatouspyelonephritisBLADDERPost-BCGPost-cauteryPost-surgicalMalakoplakiaPROSTATENon-specific granulomatousprostatitisAllergic granulomatousprostatitisPost-BCGPost-surgicalTESTESNon-specific granulomatousorchitisNeoplasia -> seminoma, lymphomaGYNECOLOGICAL TRACTOVARYPinworm (Enterobiusvermicularis)ShistoActinomyces w/ IUDCrohn’s disease (extension from bowel)Foreign body (talc, keratin from ruptured teratoma)Post-surgicalXanthogranulomatousUTERUS-ENDOMETRIUM, FALLOPIAN TUBEPinworm, ShistoCERVIXPost-surgery (necrobiotic)GISTOMACH/GI TRACT1. Crohn’s = patchy in antrum2. Ulcerative colitis (superficial)2. Vasculitis associatedAPPENDIXIdiopathicYersinia, pinworm (Enterobiusvermicularis)LIVERPrimary Biliary CirrhosisEchinococcalGranulomas is a result of chronic inflammatory reaction containing a collection of cells of monocytic series arrange in a compact mass.Cells•Macrophages•Epithelioid cells•Giant cells: Langhans giant cellsForeign body type giant cells Accumulation of macrophages · Under the influence of chemotaxisC5a, fibrinopeptides, cationic proteinsLymphokines :PDGF, TGF(beta)products of collagen brake down· By mitotic division· Immobilization and prolong survival (if the irritants are low virulent )Tuberculosis· Chronic disease common worldwide.· Causes a characteristic granulomatous inflammation · Inability of the neutrophils to kill the micro organisms due to lipoprotein coating.· Mycobacterium tuberculosis. Hominis (lungs) Bovis (Tonsils, Intestine) Spread•Droplet from patients (weeks or months)•Conjunctiva •Punctures •However need sustain contact than casual contact.Tissue damage •MT has no Endotoxins
What are viral hemorrhagic fevers?Researchers wearing protective clothing investigate the 1993 HPS outbreak.Viral hemorrhagic fevers (VHFs) refer to a group of illnesses that are caused by several distinct families of viruses. In general, the term "viral hemorrhagic fever" is used to describe a severe multisystem syndrome (multisystem in that multiple organ systems in the body are affected). Characteristically, the overall vascular system is damaged, and the body's ability to regulate itself is impaired. These symptoms are often accompanied by hemorrhage (bleeding); however, the bleeding is itself rarely life-threatening. While some types of hemorrhagic fever viruses can cause relatively mild illnesses, many of these viruses cause severe, life-threatening disease.The Special Pathogens Branch (SPB) primarily works with hemorrhagic fever viruses that are classified as biosafety level four (BSL-4) pathogens. A list of these viruses appears in the SPB disease information index. The Division of Vector-Borne Infectious Diseases, also in the National Center for Infectious Diseases, works with the non-BSL-4 viruses that cause two other hemorrhagic fevers, dengue hemorrhagic fever and yellow fever.How are hemorrhagic fever viruses grouped?VHFs are caused by viruses of four distinct families: arenaviruses, filoviruses, bunyaviruses, and flaviviruses. Each of these families share a number of features:They are all RNA viruses, and all are covered, or enveloped, in a fatty (lipid) coating. Their survival is dependent on an animal or insect host, called the natural reservoir. The viruses are geographically restricted to the areas where their host species live. Humans are not the natural reservoir for any of these viruses. Humans are infected when they come into contact with infected hosts. However, with some viruses, after the accidental transmission from the host, humans can transmit the virus to one another. Human cases or outbreaks of hemorrhagic fevers caused by these viruses occur sporadically and irregularly. The occurrence of outbreaks cannot be easily predicted. With a few noteworthy exceptions, there is no cure or established drug treatment for VHFs. In rare cases, other viral and bacterial infections can cause a hemorrhagic fever; scrub typhus is a good example.What carries viruses that cause viral hemorrhagic fevers?Viruses associated with most VHFs are zoonotic. This means that these viruses naturally reside in an animal reservoir host or arthropod vector. They are totally dependent on their hosts for replication and overall survival. For the most part, rodents and arthropods are the main reservoirs for viruses causing VHFs. The multimammate rat, cotton rat, deer mouse, house mouse, and other field rodents are examples of reservoir hosts. Arthropod ticks and mosquitoes serve as vectors for some of the illnesses. However, the hosts of some viruses remain unknown -- Ebola and Marburg viruses are well-known examples.Where are cases of viral hemorrhagic fever found?Taken together, the viruses that cause VHFs are distributed over much of the globe. However, because each virus is associated with one or more particular host species, the virus and the disease it causes are usually seen only where the host species live(s). Some hosts, such as the rodent species carrying several of the New World arenaviruses, live in geographically restricted areas. Therefore, the risk of getting VHFs caused by these viruses is restricted to those areas. Other hosts range over continents, such as the rodents that carry viruses which cause various forms of hantavirus pulmonary syndrome (HPS) in North and South America, or the different set of rodents that carry viruses which cause hemorrhagic fever with renal syndrome (HFRS) in Europe and Asia. A few hosts are distributed nearly worldwide, such as the common rat. It can carry Seoul virus, a cause of HFRS; therefore, humans can get HFRS anywhere where the common rat is found.While people usually become infected only in areas where the host lives, occasionally people become infected by a host that has been exported from its native habitat. For example, the first outbreaks of Marburg hemorrhagic fever, in Marburg and Frankfurt, Germany, and in Yugoslavia, occurred when laboratory workers handled imported monkeys infected with Marburg virus. Occasionally, a person becomes infected in an area where the virus occurs naturally and then travels elsewhere. If the virus is a type that can be transmitted further by person-to-person contact, the traveler could infect other people. For instance, in 1996, a medical professional treating patients with Ebola hemorrhagic fever (Ebola HF) in Gabon unknowingly became infected. When he later traveled to South Africa and was treated for Ebola HF in a hospital, the virus was transmitted to a nurse. She became ill and died. Because more and more people travel each year, outbreaks of these diseases are becoming an increasing threat in places where they rarely, if ever, have been seen before.How are hemorrhagic fever viruses transmitted?Viruses causing hemorrhagic fever are initially transmitted to humans when the activities of infected reservoir hosts or vectors and humans overlap. The viruses carried in rodent reservoirs are transmitted when humans have contact with urine, fecal matter, saliva, or other body excretions from infected rodents. The viruses associated with arthropod vectors are spread most often when the vector mosquito or tick bites a human, or when a human crushes a tick. However, some of these vectors may spread virus to animals, livestock, for example. Humans then become infected when they care for or slaughter the animals.Some viruses that cause hemorrhagic fever can spread from one person to another, once an initial person has become infected. Ebola, Marburg, Lassa and Crimean-Congo hemorrhagic fever viruses are examples. This type of secondary transmission of the virus can occur directly, through close contact with infected people or their body fluids. It can also occur indirectly, through contact with objects contaminated with infected body fluids. For example, contaminated syringes and needles have played an important role in spreading infection in outbreaks of Ebola hemorrhagic fever and Lassa fever.What are the symptoms of viral hemorrhagic fever illnesses?Specific signs and symptoms vary by the type of VHF, but initial signs and symptoms often include marked fever, fatigue, dizziness, muscle aches, loss of strength, and exhaustion. Patients with severe cases of VHF often show signs of bleeding under the skin, in internal organs, or from body orifices like the mouth, eyes, or ears. However, although they may bleed from many sites around the body, patients rarely die because of blood loss. Severely ill patient cases may also show shock, nervous system malfunction, coma, delirium, and seizures. Some types of VHF are associated with renal (kidney) failure.How are patients with viral hemorrhagic fever treated?Patients receive supportive therapy, but generally speaking, there is no other treatment or established cure for VHFs. Ribavirin, an anti-viral drug, has been effective in treating some individuals with Lassa fever or HFRS. Treatment with convalescent-phase plasma has been used with success in some patients with Argentine hemorrhagic fever.How can cases of viral hemorrhagic fever be prevented and controlled?With the exception of yellow fever and Argentine hemorrhagic fever, for which vaccines have been developed, no vaccines exist that can protect against these diseases. Therefore, prevention efforts must concentrate on avoiding contact with host species. If prevention methods fail and a case of VHF does occur, efforts should focus on preventing further transmission from person to person, if the virus can be transmitted in this way.Because many of the hosts that carry hemorrhagic fever viruses are rodents, disease prevention efforts include:controlling rodent populations; discouraging rodents from entering or living in homes or workplaces; encouraging safe cleanup of rodent nests and droppings. For hemorrhagic fever viruses spread by arthropod vectors, prevention efforts often focus on community-wide insect and arthropod control. In addition, people are encouraged to use insect repellant, proper clothing, bednets, window screens, and other insect barriers to avoid being bitten.For those hemorrhagic fever viruses that can be transmitted from one person to another, avoiding close physical contact with infected people and their body fluids is the most important way of controlling the spread of disease. Barrier nursing or infection control techniques include isolating infected individuals and wearing protective clothing. Other infection control recommendations include proper use, disinfection, and disposal of instruments and equipment used in treating or caring for patients with VHF, such as needles and thermometers.In conjunction with the World Health Organization, CDC has developed practical, hospital-based guidelines, titled Infection Control for Viral Haemorrhagic Fevers In the African Health Care Setting. The manual can help health-care facilities recognize cases and prevent further hospital-based disease transmission using locally available materials and few financial resources.What needs to be done to address the threat of viral hemorrhagic fevers?Scientists and researchers are challenged with developing containment, treatment, and vaccine strategies for these diseases. Another goal is to develop immunologic and molecular tools for more rapid disease diagnosis, and to study how the viruses are transmitted and exactly how the disease affects the body (pathogenesis). A third goal is to understand the ecology of these viruses and their hosts in order to offer preventive public health advice for avoiding infection.
CDC guidelinesAll pregnant women should be cultured at 35-37 weeks gestationPenicillin prophylaxis preferred, due to narrow spectrumProphylaxis recommended forPositive cervical culture for GBSGBS bacteruria during gestationPrevious infant born with invasive GBS diseaseRisk factors in absence of culture resultsGestation < 37 wksFeverROM > 18 hrProphylaxis not needed for Cesarean sections for culture positive mothers with intact membranes
PROTECTING YOURSELF FROM ZOONOTIC INFECTIONWhat is a Zoonoses?A zoonotic disease is an infection that is naturally transmitted from vertebrate animals to human beings.Many of these infections are transmitted directly but others are passed via vectors such as mosquitoes orfleas. Not all animal diseases are zoonotic and far more human illnesses result from contact with otherhumans than from animals. However, it is important for anyone working with animals to be aware of thepotential for infection and takes steps to prevent exposure. The following lists some of the morecommon or severe zoonoses and ways to help protect yourself and others from exposure.IMPORTANT RULES TO HELP YOU AVOID DEVELOPING A SERIOUS ZOONOTIC ILLNESS: Stay current on appropriate vaccinations, such as tetanus and rabies. Wash your hands frequently with antibacterial soap, especially after handling any animal andprior to eating or smoking. Wear long pants and sturdy shoes or boots. Use gloves when handling animals and when cleaning up feces, urine, or vomit. Immediately disinfect scratches and bite wounds thoroughly. Keep scratches or other abrasionscovered, especially when cleaning up after animals. Learn safe and humane animal-handling techniques and use proper equipment. Seek assistance when handling animals whose dispositions are questionable. If exposed to tick-infested areas, check your body and clothing frequently. Use tweezers andwear gloves to remove ticks, taking care not to squeeze or puncture the body of the tick. Report any bites or injuries to a supervisor and seek medical treatment as appropriate. Tell your physician that you work closely with animals, and visit him or her regularly. If you are pregnant or immunocompromised notify the lead veterinarian prior to the clinic.Discuss appropriate precautions with your physician.2COMMON ZOONOTIC INFECTIONSBartonellosis (Cat-Scratch Disease)Commonly known as cat-scratch disease (CSD), bartonellosisis is caused by the bacterium, Bartonellahenselae.The bacteria are transmitted to humans through cat scratches and bites, most likely as a result ofcontaminated flea dirt infecting the wound. Most people who get CSD are under the age of 20.Symptoms in humans include swollen lymph nodes, fever, fatigue, loss of appetite, and headache. Inextreme cases, encephalitis or other severe illnesses can develop.Kittens younger than one year old are more likely to be associated with CSD than are older cats. Theagent is transmitted between animals by flea bites. Cats are almost always asymptomatic.Since fleas are essential for transmission of the disease, flea control is key to limiting spread of thisdisease. All bites and scratches should be promptly and thoroughly washed with soap and water.CampylobacteriosisCampylobacteriosis is a bacterial infection that affects the intestinal tract and sometimes thebloodstream. Although less well known than the widely publicized gastrointestinal disease salmonellosis,campylobacteriosis is actually more common.Wild animals, especially birds, carry Campylobacter. Also, domestic animals can carry the infection.Young animals are a higher risk. Most animals are asymptomatic, but may have diarrhea with or withoutvomiting, anorexia and fever. The disease is transmitted between animals by ingestion of infected feces.Most people contract the disease by consuming contaminated food or water, such as unpasteurized milkand uncooked poultry. Infected animal can also transmit the disease and those handling ill animals areat greater risk of infection via this route. Inadequate sanitation, disease control, and personal hygienecompound the risks. Symptoms in humans include abdominal pain, cramps, fever, chills, and diarrhea.External Parasitic Infections (lice, fleas, ticks, etc.)People can contract, mite, lice or flea-related infections by coming into close physical contact withinfested animals and their bedding. Symptoms of infection will vary depending on the parasite. Someparasites (fleas, ticks) also act as vectors for more serious zoonotic diseases.Most of these parasites (mange mites, fleas, lice) that live on animals or in the environment cause only atransient infection in humans (will bite people but not likely infest or reproduce on them). The zoonoticmite disease sarcoptic mange (see below) can cause mild to severe skin infection and sometimes asecondary bacterial infection. Lice-caused pediculosis can also cause mild to severe skin irritation,which may develop into a bacterial infection when people scratch. Flea allergy dermatitis can create skinirritation and lesions in some people.Sarcoptesscabiei is an arachnid mite that burrows under the skin of the infected dog to lay eggs.Affected dogs show intense itching, rash, reddened, crusty skin, and hair loss. The ear flaps, elbows,ventral abdomen and chest, and legs are most commonly affected.Humans can contract the mite via close contact with infected animals. Signs in humans include itchy,raised rash, usually on the arms, legs, abdomen or chest. The disease is generally self-limiting inhumans as the mites will bite but do not reproduce on a human host.Note: Demodectic mange, while severe and often difficult to treat in animals, is not transmissible fromanimals to humans.3Giardiasis (also known as Beaver fever)Giardiasis is caused by a protozoal parasite (Giardiaspp) which affects the gastrointestinal tract.Both wild and domestic animals carry the disease. Animals are commonly asymptomatic, but may havediarrhea, chronic weight loss, and pale, malodorous feces. The parasite is shed in the feces and can betransmitted between animals via direct contact with infected feces, contaminated water or fomites.Although humans are much more likely to be infected via contaminated drinking water, contact withanimal feces or contaminated surfaces can bring animal care workers into frequent contact withinfectious materials. Inadequate sanitation and personal hygiene compound these risks.Although some people experience no symptoms, typical symptoms include mild or severe diarrhea,abdominal pain, nausea, and occasional weight loss. Fever is rarely present.Leptospirosis (also known as Canicola fever and Weil's disease)Caused by a spirochete (Leptospira spp.), leptospirosis is carried by domestic and wild mammals.Dogs with a history of hunting or exposure to livestock or wildlife are at increased risk. Infected dogs arecommonly asymptomatic. Severe cases can cause vomiting, anorexia, lethargy, fever, ocular/nasaldischarge, kidney and liver disease and death. The infectious agent is primarily present in urine. Themost common route of infection is through contact with contaminated water or soil.People can contract leptospirosis by consuming contaminated food or water or by coming into closecontact with an infected animal's urine. For veterinary personnel, the predominant risk is from dogs; catsare rarely infected. Although the disease is relatively rare in humans, animal care workers' close contactwith animals puts them at higher risk. Symptoms include prolonged fever, chills, weakness, abdominaland muscle pain, and sometimes jaundice and anemia. Fatality is low but the disease is especiallydangerous for the elderly, people with compromised immune systems, and people with kidney damage.Lyme DiseaseLyme disease is a tick-borne disease caused by the spirochete Borreliaburgdorferi.Wild and domestic mammals, including dogs, cats, white-tailed deer and others, serve as hosts to thedisease-carrying tick. Symptoms in animals include fever, lethargy, decreased appetite, sudden orsevere lameness, and joint swelling.Humans contract Lyme disease through a bite from a very small tick commonly referred to as a deer tick.To transmit the disease, the tick must be attached for several hours. Prompt removal of ticks from theskin is important in preventing infection.The first symptom of the disease is normally an expanding circular (or "bull's eye") rash appearing at thesite of the tick bite 2 to 30 days after the bite occurs. Flu-like symptoms (headaches, nausea, fever,muscle aches) may also appear. Left untreated, the disease may cause complications in the heart andnervous system. Arthritis, swelling, and joint pain may be recurring effects of untreated Lyme disease.Nematode (Worm) InfectionsThe nematode infections of most concern to animal care workers and pet owners are: canine roundwormdisease (visceral larva migrans, toxocariasis), hookworm disease (cutaneous larval migrans, creepingeruption) and raccoon roundworm disease (Baylisascarisprocyonis). All of these diseases are causedby parasitic worm larvae that usually infest their hosts via contaminated food sources or feces butsometimes by burrowing directly into the host's skin.Parasitic larvae can infest both wild and domestic animals. Common symptoms in animals includeanemia, weight loss and diarrhea.Humans typically acquire worm-related zoonotic diseases when they come into close contact withinfested animals or by ingesting or touching infected feces or contaminated surfaces. Infections can also4be contracted when larvae penetrates the skin. Symptoms depend on what organs the larvae migrate toand may include gastrointestinal, respiratory, dermatologic, CNS or visual symptoms.RabiesRabies is a deadly disease caused by an RNA virus (of the family Rhabdoviridae) which attacks thecentral nervous system of mammals. With rare exception, rabies is always fatal.Any warm-blooded mammal can get rabies. However, some animals, such as skunks, raccoons, andbats, are more susceptible to the virus than others. Cats and dogs, while less susceptible to rabies thanmany animals, are more likely to transmit the virus from wild animals to humans. Animals rarely afflictedwith rabies include humans, rats, squirrels, opossums and rabbits.The virus, which is present in the salivary glands of infected animals, is usually transmitted through a biteor a break in the skin, and can be transmitted through mucous membranes, but this is less likely.Because the virus shows up only intermittently in saliva, exposure to a rabid animal does not necessarilymean the virus was transmitted.Symptoms of rabies in animals can be variable. The first visible sign is often a change in behavior,ranging from depression or disorientation to aggression and violence. Several other animal diseases,such as distemper and toxoplasmosis, may mimic rabies, which further complicates potential diagnosis.The first rabies symptoms in humans mimic the flu (weakness, fatigue, lack of appetite, headache, fever).Many also report tingling at the exposure site. Symptoms progress to hyperactivity, disorientation,hallucinations, and convulsions. The disease slowly and painfully paralyzes its victims resultingeventually in death from respiratory arrest.Infected animals will show clinical signs of rabies within 10 days of the time virus is present in the saliva,which forms the basis of rationale for the standard quarantine period. Definitive diagnosis can only bemade by post-mortem antibody testing of brain tissue.All bites should be reported, and the appropriate quarantine or testing performed. Local or state publichealth department should be contacted for specific quarantine guidelines. Bite wounds should beimmediately and thoroughly cleaned with soap and water. The Center for Disease Control recommendspre-exposure vaccination and serologic testing every 2 years to ensure adequate antibody levels forthose at high risk (most veterinary personnel).Ringworm (Dermatophytosis)Ringworm is the common name given to external fungal infections of the hair and skin. Most ringworminfection in animals is caused by either Microsporumcaninum or TrichophytonmentagrophytesIn animals, ringworm infection will usually present as circular areas of hair loss and scaling. The mostcommon locations are the face, ears, feet and tail. However, infection can present differently and canmimic other dermatological conditions. Asymptomatic carriage is also possible.Infection is spread via direct contact, contaminated environment, or fomites and may be spread toanimals from infected humans. In humans, the disease presents as ring shaped areas of scaling andhair loss, with or without redness, crusting and itching.Positive or suspect animals should be isolated and handled with protective clothing. Environmentaldecontamination is essential to prevent recurrence of the disease. Without aggressive cleaning sporesmay persist and remain infectious for years. All surfaces must be cleaned, using bleach diluted at 1:10where ever possible.5Rocky Mountain Spotted FeverRocky Mountain spotted fever (RMSF) is the most severe tick-borne rickettsial illness in the UnitedStates. This disease is caused by infection with the bacterial organism Rickettsiarickettsii.The organism that causes RMSF is transmitted by the bite of an infected tick or by contamination of theskin with the contents of an attached tick when it is removed from the skin. Ticks acquire the organism byfeeding on infected small mammals which function as reservoirs for the organism. Dogs and humansalso function as reservoirs for the RMSF; however, they are incidental hosts and are the only reservoirsthat display clinical signs of disease. While the disease is generally thought to be self-limiting, recentevidence has shown that untreated RMSF may lead to death of the affected animal.In humans, initial symptoms usually appear 5-10 days after a tick bite and may include fever, nausea,vomiting, muscle or joint pain, severe headache and rash. The three important components of the clinicalpresentation are fever, rash, and a previous tick bite, although one or more of these components may notbe present. RMSF can be a severe illness, and without antibiotic treatment, the infection can be fatalLimiting exposure to ticks reduces the likelihood of Rocky Mountain spotted fever infection. It may takeseveral hours of attachment before organisms are transmitted from the tick, prompt careful inspectionand removal of crawling or attached ticks is an important method of preventing disease.SalmonellosisSalmonellosis is caused by the bacteria species Salmonella.Birds and reptiles (especially iguanas and turtles) are the animals most frequently associated withSalmonella. Wild and domestic animals, including dogs and cats, occasionally carry the disease.Diarrhea and vomiting are the most likely signs that a dog or cat may have salmonellosis. Severe casescan resemble panleukopenia or parvo and can lead to septicemia and death.Most people have a much greater risk of contracting salmonella from eating undercooked chicken andother meat products than they do from contact with animals. Careful hygiene is important though,particularly when handling high-risk animals.In humans, symptoms include diarrhea (usually watery and occasionally bloody), nausea, vomiting,fever, chills, and abdominal cramps. If the bacteria leaves the bloodstream and enters the centralnervous system, meningitis/encephalitis may develop.ToxoplasmosisToxoplasmosis is caused by the single-celled protozoan Toxoplasmagondii. The organism resides inthe intestinal tract of cats and in the tissues of many rodents and animals raised for human food.Although cats are the only animals that can shed the parasite's eggs (oocysts) in their feces, T. gondiialso resides in animals' tissues and is released when other animals or humans consume that tissue.Most cats are asymptomatic. When symptoms are apparent, they usually include vague signs likediarrhea, weight loss, and transient fever.People are most commonly infected as a result of eating raw or undercooked meat, but can also get thedisease if they ingest food or water contaminated with cat feces.Most cases of clinical disease resemble the flu; symptoms include fever, enlarged lymph nodes, fatigue,headache, and sore throat. However, although many people are infected with T. gondii, most healthypeople develop minimal or no symptoms. People likely to develop clinical symptoms are children andpeople with compromised immune systems. Pregnant women who become infected with toxoplasmosisfor the first time while pregnant risk infecting their fetus, which can result in stillbirths, spontaneousabortions, and birth defects. Once inside the body, the parasite never leaves it. Although in healthypeople the parasite remains inactive, it can "reactivate" in immunocompromised individuals.Adapted from 'Controlling Zoonotic Diseases in Your Shelter' Animal Sheltering/The HSUS 1996
Primary TBIn primary TB, a person has become infected with the TB bacteria but often is not aware of it, since this stage of the disease does not produce noticeable symptoms. Primary TB is not contagious in this early stage. Macrophages, immune cells that detect and destroy foreign matter, ingest the TB bacteria and transport them to the lymph nodes where they may be inhibited, destroyed, or they may multiply. (Primary and Secondary TB, Early Symptoms, Primary and Secondary Tuberculosis, Early Stage) If the bacteria multiply, active primary tuberculosis will develop. Symptoms include coughing, night sweats, weight loss, and fever. A chest X ray may show shadows in the lung or fluid collection between the lung and its lining. If the bacteria are inhibited, rather than destroyed, the immune cells and the bacteria form a mass known as a granuloma or tubercle. In effect, the immune cells form a wall around inactive bacteria. As long as the immune system remains strong, the TB bacteria remain walled off and inactive. The tubercle gradually collects calcium deposits to form what is known as a Ghon focus. These initial tubercles in the lung usually heal, leaving permanent scars that appear as shadows in chest X rays. At this initial stage of TB, the disease does not progress, but bacteria may remain dormant in the body for many years. If the immune system becomes weakened, the tubercle opens, releasing the bacteria, and the infection may develop into secondary TB. (Primary and Secondary TB, Early Symptoms, Primary and Secondary Tuberculosis, Early Stage) Secondary TBIn secondary TB, the formerly dormant bacteria multiply and destroy tissue in the lungs. They also may spread to the rest of the body via the bloodstream. Fluid or air may collect between the lungs and the lining of the lungs, while tubercles continue to develop in the lung, progressively destroying lung tissue. Coughing of blood or phlegm may occur. At this secondary stage, carriers of TB can infect others. (Primary and Secondary TB, Early Symptoms, Primary and Secondary Tuberculosis, Early Stage)
a form of leprosy chiefly affecting the nerves, marked by hyperesthesia succeeded by anaesthesia, and by paralysis, ulceration, and various trophicdisturbances, terminating in gangrene and mutilation. The more severe form of leprosy, lepromatous leprosy, includes symmetric skin thickening and nodules. This is also called anergic leprosy, because of the unresponsiveness (anergy) of the host immune system. Cooler areas of skin, including the earlobes and feet, are more severely affected than warmer areas, such as the axilla and groin.In lepromatous leprosy, damage to the nervous system comes from widespread invasion of the mycobacteria into Schwann cells and into endoneural and perineural macrophages.In advanced cases of lepromatous leprosy, Mycobacterium leprae is present in sputum and blood.
Syphilis - primaryDefinition Syphilis is a frequently diagnosed sexually transmitted disease.Alternative Names Primary syphilisCauses Syphilis is a sexually transmitted, infectious disease caused by the spirochete Treponemapallidum. This bacteria causes infection when it gets into broken skin or mucus membranes, usually of the genitals. It is most often transmitted through sexual contact, although it also can be transmitted in other ways.Syphilis occurs worldwide. Syphilis is more common in urban, rather than rural, areas, and the number of cases is rising most rapidly in men who have sex with men. Young adults, ages 15-25, are the highest-risk population. People have no natural resistance to syphilis.Because people may be unaware that they are infected with syphilis, many states require tests for syphilis before marriage. All pregnant women who receive prenatal care are screened for syphilis to prevent the syphilis infection from passing from the mother to the newborn (congenital syphilis).Syphilis has three stages:Primary syphilisSecondary syphilisTertiary syphilisSecondary syphilis, tertiary syphilis, and congenital syphilis are not seen as often in the United States as they were in the past because of the availability of free, government-run sexually transmitted disease clinics, screening tests for syphilis, public education about STDs, and prenatal screening.Symptoms Primary syphilis symptoms include:Chancre -- a small, painless open sore or ulcer on the genitals, mouth, skin, or rectum that should heal by itself in 3-6 weeksEnlarged lymph nodes in the area containing the chancreThe bacteria continue to multiply in the body, but there is little outward evidence of disease until the second stage.Exams and Tests Dark field examination of fluid from soreSerumRPR or serumVDRL (used as screening tests to detect syphilis infection -- if positive, one of the following tests will be needed to confirm the diagnosis:) FTA-ABS (fluorescent treponemal antibody test)MHA-TPTreatment Syphilis can be treated with antibiotics, such as penicillin G benzathine, doxycycline, or tetracycline (for patients who are allergic to penicillin). Length of treatment depends on the extent of the syphilis and factors such as the patient's overall health.For treatment of syphilis during pregnancy, penicillin is the drug of choice. Tetracycline cannot be used because it is dangerous to the fetus, and erythromycin may not prevent congenital syphilis in the fetus. People who are allergic to penicillin should ideally be desensitized to it, then treated with penicillin.Several hours after getting treatment for the early stages of syphilis, people may experience Jarish-Herxheimer reaction, which is caused by an immune reaction to the breakdown products of the infection.Symptoms of this reaction include:ChillsFeverGeneral feeling of being ill (malaise)HeadacheJoint achesMuscle achesNauseaThese symptoms usually disappear within 24 hours.Follow-up blood tests must be done at 3, 6, 12, and 24 months to ensure that the infection is gone. Avoid sexual contact when the chancre is present, and use condoms until two follow-up tests have indicated that the infection has been cured.All sexual partners of the person with syphilis should also be treated. Syphilis is extremely contagious in the primary and secondary stages.Outlook (Prognosis) Syphilis can be completely cured if diagnosed early and treated thoroughly. Possible Complications Cardiovascular syphilisCongenital syphilisNeurosyphilisSecondary syphilisSyphilitic meningitisTertiary syphilisWhen to Contact a Medical Professional Call for an appointment with your health care provider if you have symptoms of syphilis.If you have had intimate contact with a person who has syphilis or any other STD, or have engaged in any high-risk sexual practices, including having multiple or unknown partners or using intravenous drugs, contact your doctor or get screened in an STD clinic.Prevention If you are sexually active, practice safe sex and always use a condom.All pregnant women should be screen for syphilis.Syphilis - secondaryDefinition Secondary syphilis is the second stage of the sexually transmitted disease syphilis. This stage is the most contagious.Alternative Names Secondary syphilisCauses Syphilis is a sexually transmitted infectious disease caused by the spirochete Treponemapallidum. Syphilis has three main stages:Primary syphilisSecondary syphilisTertiary syphilisThis article focuses on secondary syphilis.About a third of untreated individuals with primary syphilis will develop secondary syphilis. This usually occurs at about 2 to 8 weeks after the appearance of the original painless sore (chancre). Sometimes, the sore may still be present.In secondary syphilis, the bacteria has spread into the bloodstream.Symptoms The most common symptom is a skin rash, which varies in appearance, yet frequently involves the palms and soles. Lesions called mucous patches may be seen in or on the mouth, vagina, or penis.Moist, warty patches may develop on the genitalia or skin folds. These are called condylomatalata.During secondary syphilis, additional symptoms such as fever, general ill feeling, loss of appetite, muscle aches, joint pain, enlarged lymph nodes, and hair loss may occur.Exams and Tests Serum VDRL or serum RPR (used as screening tests). If these are positive, one of the following will need to be done to confirm the diagnosis: FTA-ABSMHA-TPTreatment Antibiotics are used to treat syphilis. The antibiotic of choice is penicillin, yet doxycycline may be used as an alternative in individuals with a penicillin allergy.For treatment of syphilis during pregnancy, penicillin is the drug of choice. Tetracycline cannot be used because it is toxic to the developing baby, and erythromycin may not prevent spread of the infection to the developing baby (congential syphilis). People allergic to penicillin should be desensitized to it before treatment.You must have follow-up blood tests at 3 and 6 months (and later if needed) to make sure the infection is gone. You should avoid sexual conduct until two follow-up tests show that the infection has been cured. Syphilis is extremely contagious in the primary and secondary stages.Several hours after treatment, some people have a reaction called Jarish-Herxheimer reaction. Symptoms of this reaction include:ChillsFeverGeneral feeling of being illGeneral joint achesGeneral muscle achesHeadacheNauseaThese symptoms usually disappear within 24 hours.Syphilis is a reportable infection -- that means that doctors must reported any cases of syphilis to public health authorities, so that potentially infected sexual partners may be identified and treated.Outlook (Prognosis) Secondary syphilis can be completely cured if diagnosed early and treated effectively. While it usually goes away within weeks, in some cases it may last up to 1 year. Without treatment, up to one-third of patients will develop late complications of syphilis.Possible Complications The complications of syphilis are related to the development of the syndromes associated with tertiary syphilis:Cardiovascular complications (aortitis and aneurysms)Destructive lesions of the skin and bones (gummas)NeurosyphilisIn addition, untreated secondary syphilis during pregnancy may spread the disease to the developing baby. This is called congenital syphilis.When to Contact a Medical Professional Notify your health care provider if you develop signs or symptoms of syphilis. Several conditions may have similar symptoms, so you will need to have a complete medical exam.If you have had intimiate contact with a person who has syphilis or any other STD, or have engaged in any high-risk sexual practices, including have multiple or unknown partners, or have used intravenous drugs, contact your doctor or get screened at at STD clinic or health department clinic.Prevention If you are sexually active, practice safe sex and always use condoms.All pregnant women should be screened for syphilis.Syphilis - tertiaryDefinition Tertiary syphilis is a late phase of the sexually transmitted disease syphilis, caused by the spirochete Treponemapallidum.Alternative Names Late syphilis; Tertiary syphilisCauses Syphilis is a sexually transmitted, infectious disease caused by the spirochete Treponemapallidum.Syphilis has three main stages:Primary syphilisSecondary syphilisTertiary syphilisThis article focuses on tertiary syphilis. Tertiary syphilis can follow the initial infection (primary syphilis) by 3 to 15 years.In tertiary syphilis, the infection-causing organisms have continued to grow for years. Pockets of damage, or lesions, affects various tissues such as the bones, skin, nervous tissue, heart, and arteries. These areas are called gummas, and are very destructive.Tertiary syphilis is less frequently seen today than in the past because of early detection and adequate treatment.Symptoms Symptoms of tertiary syphilis depend on which organ systems have been affected. They vary widely and are difficult to diagnose. In individuals with tertiary syphilis, the primary and secondary stages of syphilis usually have been long forgotten. Medical findings of aortic aneurysms and neurological problems require astute diagnostic ability to link them to syphilis. Some of the symptomatic problems are listed below.Cardiovascular syphilis which affects the aorta and causes aneurysms or valve diseaseCentral nervous system disorders (neurosyphilis)Infiltrative tumors of skin, bones, or liver (gumma)Exams and Tests VDRL or RPR blood tests are used as screening tests. If they are positive, one of the following is needed to confirm the diagnosis of syphilis:FTA-ABS (fluorescent treponemal antibody test)MHA-TPSpinal fluid examination in neurosyphilis shows signs of meningitis.Treatment The treatment of syphilis is determined by the length of time the person has been infected.Syphilis can be treated with antibiotics such as penicillin, G benzathine, doxycycline, or tetracycline (for patients who are allergic to penicillin). Length of treatment depends on the extent of the infection and factors such as the person's overall health.For treating syphilis during pregnancy, only penicillin is recommended. Tetracycline cannot be used because it is toxic to the fetus, and erythromycin may fail to prevent the spread of the infection (congenital syphilis) to the fetus. Penicillin-allergic individuals should be desensitized and then treated with penicillin.Several hours following treatment of early stages of syphilis, some individuals may undergo a febrile reaction called Jarisch-Herxheimer reaction. This is thought to be caused by the release into the circulation of material from dead or dying spirochetes. Symptoms of this reaction include:ChillsFeverGeneral feeling of being ill (malaise)Generalized joint aches (arthralgia)Generalized muscle aches (myalgia)HeadacheNauseaThese symptoms usually disappear within 24 hours.Follow-up blood tests must be done 3, 6, 12, and 24 months after treatment to ensure that the infection has been eliminated.Individuals with primary or secondary syphilis should abstain from sex until they have been treated. Syphilis is extremely contagious in the primary and secondary stages.Outlook (Prognosis) Late syphilis may be permanently disabling and may lead to death.Possible Complications AneurysmsHeart valve diseaseNeurosyphilisSyphilis infection of the heartWhen to Contact a Medical Professional Untreated syphilis can result in serious health problems. It is very important that you tell your doctor if you think you might have had syphilis, even if it was many years ago.Prevention If you are sexually active, practice safe sex and always use a condom.All pregnant women should be screen for syphilis.
MalariaThe undisputed king of parasite-caused diseases, Malaria is a serious human disease that weakens an infected individual and may easily lead to death. It is caused by the Sporozoanspecies known as Plasmodium. (Sporozoans are members of the parasitic Phylum Sporozoa (spohr-oh-ZOH-uh), one of several sub-groups of eukaryotic organisms in the (biological) kingdom Protista). Plasmodium is carried by the Anopheles (uh-NAHF-uh-leez) mosquito.When an infected mosquito bites a human, some of its saliva, which contains spores of the parasite, is injected into the bloodstream. Once inside the body, Plasmodium infects liver cells and then red blood cells. Plasmodium grows rapidly within the infected cells and eventually causes these cells to burst at intervals of 48 or 72 hours. When millions of parasite-filled red blood cells burst, they dump large amounts of toxins into the bloodstream. The toxins produce chills and fever- the symptoms of malaria.The disease is transmitted back to the mosquito if a mosquito bites a human infected with malaria. The blood that the mosquito swallows contains Plasmodium. In the insect's digestive system, Plasmodium grows rapidly and penetrates the insect's entire body, including the salivary glands. After a time the infected insect contains active Plasmodium spores in its saliva and is able to pass the infection on to another human. Every year, more than 500 million people suffer from Malaria and more than a million people die from it. Although drugs such as chloroquinine are effective against some forms of the disease, many strains of malaria-causing Plasmodium sporozoans are resistant to these drugs. To date, the most effective way to control malaria is to destroy breeding areas for Anopheles mosquitoes. This interrupts the life cycle of Plasmodium and thus prevents the spread of malaria. Sleeping SicknessSleeping sickness or human African trypanosomiasis is a parasitic disease of people and animals, caused by protozoa of species Trypanosomabrucei and transmitted by the tsetse fly. The disease is endemic in certain regions of Sub-Saharan Africa, covering about 36 countries and 60 million people. It is estimated that 50,000 to 70,000 people are currently infected, the number having declined somewhat in recent years. Three major epidemics have occurred in recent history, one lasting from 1896–1906 and the other two in 1920 and 1970. In 2008 there was an epidemic in Uganda.Clinical featuresSymptoms begin with fever, headaches, and joint pains. As the parasites enter through both the blood and lymph systems, lymph nodes often swell up to tremendous sizes. Winterbottom's sign, the telltale swollen lymph nodes along the back of the neck may appear. If untreated, the disease slowly overcomes the defenses of the infected person, and symptoms spread to include anemia, endocrine, cardiac, and kidney diseases and disorders. The disease then enters a neurological phase when the parasite passes through the blood-brain barrier. The symptoms of the second phase give the disease its name; besides confusion and reduced coordination, the sleep cycle is disturbed with bouts of fatigue punctuated with manic periods progressing to daytime slumber and nighttime insomnia. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma and death. Damage caused in the neurological phase can be irreversible. In addition to the bite of the tsetse fly, the disease is contractible in the following ways:1) Mother to child infection: the trypanosome can cross the placenta and infect the fetus, causing perinatal death. 2) Laboratories: accidental infections, for example, through the handling of blood of an infected person and organ transplantation, although this is uncommon. 3) Blood transfusion 4) Sexual contact .
No effective treatment. Available drugs only kill extracellular parasites. Most successful treatmentduring acute phase - about a 60% success. Benznidazole and Nifurtinox: current drugs of choice. Required daily for up to 2 months ormore. Hospitalization may be needed because of adverse effectsTrypanosomacruzi South and Central AmericaSuramin, pentamidine and berenil: can cure infection if given before invasion of nervous system. Difluoromethylornithine (DMFO) even if the parasite has invaded the brain.Trypanosomabruceigambiense West Africa
Intestinal amoebiasisThe most common type of amoebic infection is the asymptomatic passage of cysts.Symptomatic patients initially have lower abdominal pain and diarrhoea and later develop dysentery (with blood and mucus in stool).Amoebic colitis with dysentery: loose stools with fresh blood. Patient is usually generally well with mild or moderate abdominal pain. Symptoms often fluctuate over weeks or even months with patient becoming debilitated.Abdominal tenderness in one or both iliac fossae but may be generalised. Palpably thickened gut. Low fever. Abdominal distension in more severely ill patients passing relatively small amounts of stool sometimes.Amoebic colitis without dysentery: change in bowel habit, blood stained stools, flatulence and colicky pain, tenderness in right iliac fossa or other places over colon. May disappear or progress to dysentery.Rectal bleeding: may occasionally be only sign, with or without tenesmus (common in children).Amoeboma: Abdominal mass, which is usually in right iliac fossa.May be painful and tender.Fever, altered bowel habit and there may be intermittent dysentery.May be symptoms of partial or intermittent bowel obstruction.Fulminant colitis: more likely in children and patients taking steroids; high grade fever, severe abdominal pain, increasing distension of abdomen with vomiting plus watery diarrhoea. Absent bowel sounds. X-ray may show free peritoneal gas with acute gaseous dilatation of the colon.Localised perforation and appendicitis: deep ulcer may cause sudden perforation with peritonitis or may leak causing pericolic abscess or retroperitoneal infection. May also resemble simple appendicitis, often with signs of dysentery.Hepatic amoebiasisUsually no current and often no history of dysentery.Usually occurs within 8 weeks to 1 year of infection.Presents with sweating and pyrexia, painful liver or diaphragm together with weight loss often appearing insidiously, but pain may appear abruptly.Fever is typically remitting with prominent evening rise with brief rigors and profuse sweatingOften anaemia and dry painful cough.Liver enlargement with localised tenderness in right hypochondrium, epigastrium and intercostal spaces overlying liver.May find epigastric mass from left-lobe lesion.Upward enlargement may cause bulging of right chest wall with raised upper level of liver dullness on percussion. May hear reduced breath sounds or crepitations at right lung base.Abscess may extend into adjacent structures, usually the right chest, peritoneum and pericardium. If extends into lung produces hepatobronchial fistula with expectoration of brownish, necrotic liver tissue. May also cause peritonitis, pericarditis, brain abscess or genitourinary disease.
Perivascular cuffing is infiltrated lymphocytes and plasma cells. Perivascular cuffing causes thickening of the pia-arachnoid due to the lymphocytes and plasma cells infiltrating the area.The inflammation subsequently invades the Virchow-Robin spaces surrounding the blood vessels that enter the brain. During the protractred course of the Gambian disease, the vessels become progressively surrounded by the same types of cell as the affected meninges, forming the lesion termed perivascularcuffing. Both the cuffs and the surrounding brain parenchyma frequently contain proliferations of microglia and astrocytes.
The way that a pathogen (virus, bacteria, protozoa, etc, that causes disease) travels successfully from one host to another is referred to as the mode of transmission. There are several different modes of transmission which different pathogens use to jump from one host to another. Usually, pathogens can only use one or few possible modes of transmission. For instance, HIV (the virus that causes AIDS) cannot travel through the air from host to host. It can only be transmitted by direct contact with body fluids such as blood or semen. In order to help you identify the mode of transmission used by the pathogen responsible for this outbreak, you will need to think about which of the following factors are shared by infected or sick hosts and which factors are common to non-infected or healthy hosts. Look for a factor or factors that are shared by all of the infected hosts. 1.) Exposure to breathing exhaled particles from an infected person2.) Direct contact with body fluids such as blood or semen from infected person3.) Contact with a potentially infected animal vector (animal bite, handling of animal, exposure to animal urine, feces, or blood)4.) Consumption of potentially contaminated food or water5.) Exposure to insect bitesBased on the information from your interviews and the guidance in the tutorial, which of the following do you think best describes the likely mode of transmission of the disease in this outbreak? A. Transmitted through consumption of potentially contaminated food or water B. Transmitted through contact with a potentially infected animal vector C. Transmitted to new host via exposure to insect bites Climate and topography are crucial determinants of the distribution of helminth infections (31). Helminths transmitted by vectors are limited to landscapes in which host and vector come together in the same habitat, resulting highly focal distribution. For example, the distribution of schistosomiasis reflects the biotic and abiotic features (i.e., climatic, physical, and chemical factors) that affect the survival and development of the snail vector (32). In the case of onchocerciasis, the distribution and incidence of the disease are limited by biogeographic variations favorable to exposure to the blackfly vectors (33, 34). Soil-transmitted helminths are highly affected by surface temperature (35), altitude, soil type, and rainfall (36, 37).
Doctors use thick and thin blood smears to determine whether you have malaria. If one test is negative and no parasites are found, you will have repeated blood smears every 8 hours for a couple of days to confirm that there is no malaria infection.Blood smears are taken most often from a finger prick. Thick and thin blood smears will let doctors know the percentage of red blood cells that are infected (parasite density) and what type of parasites are present.Recommended Related to Infectious DiseasesUnderstanding Rheumatic Fever -- SymptomsFever A red, raised, lattice-like rash, usually on the chest, back, and abdomen Swollen, tender, red, and extremely painful joints -- particularly the knees or ankles Nodules, or small protuberances, over the swollen joints Sometimes, weakness and shortness of breath caused by heart involvement Sometimes, uncontrolled movements of arms, legs, or facial muscles called chorea. These symptoms often begin one to six weeks after a strep throat infection has appeared to clear up....Read the Understanding Rheumatic Fever -- Symptoms article > >A thick blood smear is a drop of blood on a glass slide. Thick blood smears are most useful for detecting the presence of parasites because they examine a larger sample of blood. (Often there are few parasites in the blood at the time the test is done.)A thin blood smear is a drop of blood that is spread across a large area of the slide. Thin blood smears helps doctors discover what species of malaria is causing the infection.Why It Is DoneTo date, microscopic examination of thick and thin blood smears is the easiest and most reliable test for malaria.
Microbiologist Robert Koch was born in 1843. Koch's postulates are a series of ground rules to determine whether a given organism can cause a given disease. Koch theorized that a pathogen must be: found in all cases of the disease examinedprepared and maintained in a pure culturecapable of producing the original infection, even after several generations in cultureretrievable from an inoculated animal and cultured againFor all their lingering influence, Koch's postulates never anticipated the era of the human metagenome in which thousands of difficult or impossible-to-culture species of bacteria contribute to a single disease state. Koch's century-old ideas have held science back from understanding how chronic disease occurs because they make no provision for these facts. The Marshall Pathogenesis is consistent with mounting evidence that Koch's postulates no longer apply to discerning the vast amounts of microbes in the human body. Legacy of Koch – a false sense of confidenceAccording to T.D. Brock at the American Society of Microbiology,1 attempts to rigidly apply Koch’s postulates to the diagnosis of viral diseases may have significantly impeded the early development of the field of virology. It also impeded the understanding of chronic disease. In 1932, Razumov noted a large discrepancy between the viable plate count and total direct microscopic count of bacteria taken from aquatic habitats,2 yet his work was dismissed, underestimate, or both – undoubtedly because it was not consistent with Koch's postulates. The faithful adherence to Koch's ideas about disease has led researchers to overestimate their comprehension of how pathogens cause disease. For most of the twentieth century, the predominant feeling about the treatment, control and prevention of infectious diseases was optimism. Mitchell L. Cohen3In 1931, Henry Sigerist wrote, “Most of the infectious diseases … have now yielded up their secrets…. Many illnesses … had been completely exterminated; others had [been brought] largely under control….”4 Between 1940 and 1960, the development and successes of antibiotics and immunizations added to this optimism, and in 1969, Surgeon General William H. Stewart told the United States Congress that it was time to “close the book on infectious diseases.”5With “victory” declared, increasing emphasis was directed at the “non-infectious” diseases such as cancer and heart disease. Often, research on infectious disease or activities on their prevention and control were de-emphasized and resources were reduced or eliminated. As recently as the 1980s, pharmaceutical companies, believing that there were already enough antibiotics, began reducing the development of new drugs or redirecting it away from antibiotics.67Still valid?Robert Koch created a series of ground rules to determine whether a given organism can cause a given disease.When someone talks about imbalance of humors of the miasmic origin of disease, I always detect among listeners the amused tolerance a parent gives to an explanation from his 3-yr-old son. A discourse on Koch’s postulates, on the other hand, is treated with great solemnity. In this light, my premise that there is no more dangerous half-truth among students of disease today than the postulates of Koch may be considered sacrilegious. Robert P. Hanson8As early as the 19th century, researchers realized that viruses invalidate Koch’s postulates because they require another living cell in order to replicate. The fact that scientists are still trying to apply Koch’s postulates to bacteria is causing an even greater array of problems. For one, bacteria in the L-form (also known as cell wall deficient bacteria) cannot be easily grown in the lab and can only be studied in conditions that mimic those of the human body. As Gerald Domingue, Professor Emeritus at Tulane University states, “When it comes to L-form bacteria, Koch’s postulates cannot be fulfilled because it is impossible to duplicate all the variables involved in disease expression.” It is already widely accepted that some species of bacteria cause disease despite the fact that they do not fulfill Koch’s Postulates since Mycobacterium leprae and Treponemapallidum, (which are implicated in leprosy, and syphilis respectively) cannot be grown in pure culture medium. Another problem with the postulates - and perhaps its most significant liability - is that the rules fail to successfully account for horizontal gene transfer. Horizontal gene transfer is a process in which organisms swap genetic material, a common biological process which blurs the distinction between one organism and the next. Recall that Koch postulated that one pathogen caused one disease. Rethinking KochLife has changed since the 1880s when Robert Koch elucidated his guidelines, later to be called Koch’s postulates, for determining whether a microorganism is the cause of a disease. The horse-drawn buggy bumping over dirt roads has been replaced by the computer-assisted automobile speeding along paved highways. It would be absurd to expect modern cars to abide by trafﬁc rules and standards designed for horse-drawn carriages. Yet, many continue to hold Koch’s postulates as the unchanging standard for determining causation in medicine, despite a revolution in biotechnology and leaps in medical knowledge. Recent ﬁndings based on the application of new technologies, especially in the ﬁelds of microbiology and infectious disease, demand a renewed dialogue on proof of causation and revised guidelines for deﬁning a causal relationship between a microbe and a disease. David N. Fredricks and David A. Relman9Koch's contributions were substantial, but his ideas preceded any understanding of genetics or of horizontal gene transfer and made no provision for organisms that were not genetically distinct. The blind adherence to Koch's postulates precludes a more nuanced understanding of disease: it is in fact a group of genetically indistinct organisms, a metagenomicmicrobiota, which may cause and drive chronic disease. In a 2005 Lancet paper, Brogdenet al. point to the existence of dozens of polymicrobial diseases, caused by combinations of viruses, bacteria, fungi, and parasites.10 In these infections, the presence of one micro-organism generates a niche for other pathogenic micro-organisms to colonise, one micro-organism predisposes the host to colonisation by other micro-organisms, or two or more non-pathogenic micro-organisms together cause disease. This topic is discussed further in the article Successive infection and variability in disease.
From the perspective of infectious diseases, vectors are the transmitters of disease-causing organisms that carry the pathogens from one host to another. By common usage, vectors are considered to be invertebrate animals, usually arthropods. Technically, however, vertebrates can also act as vectors, including foxes, raccoons, and skunks, which can all transmit the rabies virus to humans via a bite. Arthropods account for over 85 percent of all known animal species, and they are the most important disease vectors. Arthropods may affect human health either directly by bites, stings, or infestation of tissues, or indirectly through disease transmission. Several genera of arthropods play a role in human disease, but mosquitoes and ticks are the most notable disease vectors. The most significant mode of vector-borne disease transmission is by biological transmission by blood-feeding arthropods. The pathogen multiplies within the arthropod vector, and the pathogen is transmitted when the arthropod takes a blood meal. Mechanical transmission of disease agents may also occur when arthropods physically carry pathogens from one place or host to another, usually on body parts.The transmission of vector-borne diseases to humans depends on three different factors: the pathologic agent; the arthropod vector; and the human host (see Figure 1).The majority of vector-borne diseases survive in nature by utilizing animals as their vertebrate hosts, and are therefore zoonoses. For a small number of zoonoses, such as malaria and dengue, humans are the major host, with no significant animal reservoirs. Intermediary animal hosts often serve as a reservoir for the pathogens until susceptible human populations are exposed. The vector receives the pathogen from an infected host and transmits it either to an intermediary host or directly to the human host. The different stages of the pathogen's life cycle occur during this process and are intimately dependent upon the availability of suitable vectors and hosts. Key components that determine the occurrence of vector-borne diseases include: (1) the abundance of vectors and intermediate and reservoir hosts; (2) the prevalence of disease-causing pathogens suitably adapted to the vectors and the human or animal host; (3) the local environmental conditions, especially temperature and humidity; and (4) the resilience behavior and immune status of the human population.Vector-borne diseases are prevalent in the tropics and subtropics and are relatively rare in temperate zones, although climate change could create conditions suitable for outbreaks of diseases such as Lyme disease, Rocky Mountain spotted fever, malaria, dengue fever, and viral encephalitis in temperate regions. There are different patterns of vector-borne disease occurrence. Parasitic and bacterial diseases, such as malaria and Lyme disease, tend to produce a high disease incidence but do not cause major epidemics. An exception to this rule is plague, a bacterial disease that does cause outbreaks. In contrast, many vector viral diseases, such as Yellow fever, dengue, and Japanese encephalitis, commonly cause major epidemics.There has been a worldwide resurgence of vector-borne diseases since the 1970s including malaria, dengue, Yellow fever, louse-borne typhus, plague, leishmaniasis, sleeping sickness, West Nile encephalitis, Lyme disease, Japanese encephalitis, Rift Valley fever, and Crimean-Congo hemorrhagic fever. Reasons for the emergence or resurgence of vector-borne diseases include the development of insecticide and drug resistance; decreased resources for surveillance, prevention and control of vectorborne diseases; deterioration of the public health infrastructure required to deal with these diseases; unprecedented population growth; uncontrolled urbanization; changes in agricultural practices; deforestation; and increased travel. Changes have been documented in the distribution of important arthropod disease vectors. The yellow fever mosquito, Aedesaegypti has reestablished in parts of the Americas where it had been presumed to have been eradicated; the Asian tiger mosquito, Aedesalbopictus, was introduced into the Americas in the 1980s and has spread to Central and South America; and the blacklegged tick, Ixodesscapularis, an important transmitter of Lyme disease and other pathogens, has gradually expanded its range in parts of eastern and central North America.Control measures for vector-borne diseases are important because most are zoonoses that are maintained in nature in cycles involving wild animals and are not amenable to eradication. Therefore, control methods generally focus on targeting the arthropod vector. These include undertaking personal protective measures by establishing physical barriers such as house screens and bed nets; wearing appropriate clothing (boots, apparel that overlap the upper garments, head nets, etc.); and using insect repellents. Environmental modification to eliminate specific breeding areas, or chemical biological control measures to kill arthropod larvae or adults may also be undertaken. Areas such as ports and airports should be rigidly monitored, with control measures utilized to preventFigure 1important arthropod disease vectors from entering the country. Some efforts to control vectorborne diseases focus on the pathogen. For example, there are vaccines available for diseases such as Yellow fever, tick-borne encephalitis, Japanese encephalitis, tularemia, and plague. The vertebrate host and/or reservoir may also be the target for control measures. For example, vaccination of fox against rabies in Europe and Canada is an effective means to reduce the threat of rabies. In addition, reduction of host reservoirs, such as rodents and birds, from areas of human habitation may lessen the risk for contracting certain vectorborne diseases such as plague and St. Louis encephalitis.It is clear that people will always have to live with vector-borne diseases, but maintenance of a strong public health infrastructure and undertaking research activities directed at improved means of controlossibly utilizing biological and genetic-based strategies, combined with the development of new or improved vaccines for diseases such as malaria, dengue and Lyme diseasehould lessen the threat to human health.
Opsonization is a term that refers to an immune process where particles such as bacteria are targeted for destruction by an immune cell known as a phagocyte. The process of opsonization is a means of identifying the invading particle to the phagocyte. Without the opsonization process the recognition and destruction of invading agents such as bacteria would be inefficient.The process of opsonization begins when the immune system recognizes a particle (e.g., a bacterium) as an invader. The recognition stimulates the production of antibodies that are specific for the antigenic target. Certain antibody molecules are stimulated to bind to the surface of the particle. Typically, the binding molecules are a type of antibody classified as IgG. As well, proteins involved in the complement-mediated clearance of foreign material, specifically a protein designated C3b, can bind to the surface of the foreign object. Proteins such as IgG and C3b, which can promote opsonization, are designated as opsonins.When the IgG antibodies bind to the invading bacterium, the binding is in a specific orientation. An antibody is somewhat "Y" shaped. The binding of IgG to the bacterium is via the branching arms of the "Y." The stalk of the molecule, which is termed the Fc region, then protrudes from the surface. The Fc region is recognized by a receptor on the surface of an immune cell called a phagocyte. When the Fc region is bound to the phagocytic receptor the invading particle is taken into the phagocyte and enzymatically digested.The Cb3 complement protein can bind in a nonspecific manner to an invading particle. Phagocytes also contain surface receptors that recognize and bind Cb3. As with IgG, the binding of Cb3 to the phagocytes triggers a process whereby the invading particle is engulfed, surrounded, and taken inside the phagocytic cell for destruction.Examples of phagocytic cells that can participate in opsonization are neutrophils and monocytes.Bacteria that are associated with the development of infections typically possess a capsule, which is a layer of carbohydrate material. The capsular material encases the bacterial cell. The carbohydrate is not recognized as readily by the immune machinery of the body as is protein. As well, the penetration of antibodies through the capsule network to the surface of the bacterium is impeded. Thus, possession of a capsule can dampen the opsonization response.
30% HIV infected people have HEP C70-90% HIV infected people have HEP Bhttp://hivinsite.ucsf.edu/InSite?page=kb-05-03-04 The most common human parasites are soil-transmitted helminths (Ascarislumbricoides, Trichuristrichiura, and the hookworms (Ancylostomaduodenale and Necatoramericanus), Plasmodium spp., Schistosoma spp. and lymph-dwelling filariae, each allegedly infecting between 100 and 800 million people (2). Dozens of further common human parasites are known (3), e.g. a host of different intestinal protozoa, members of the genera Leishmania, Typanosoma, Taenia, Trichinella, Strongyloides and Echinococcus, a diversity of trematodes dwelling in the hepato-biliary, respiratory and digestive systems, Tungapenetrans, lice, etc. Some of them infect sizable fractions of local populations or occur across many countries.
For instance, in 2006, 27 percent of new cases of HIV infection occurred in women. Intravenous drug users accounted for 12 percent of new cases. These numbers give a glimpse of the impact that HIV and AIDS continue to have.http://www.livestrong.com/article/196681-aids-vs-hiv-diagnosis/
Used to detect proteins afterelectrophoretic separation on polyacrylamide gels.
This stain is used for the demonstration of glycogen. Tissue sections are first oxidized by periodic acid. The oxidative process results in the formation of aldehyde groupings through carbon-to-carbon bond cleavage. Free hydroxyl groups should be present for oxidation to take place. Oxidation is completed when it reaches thealdehyde stage. The aldehyde groups are detected by the Schiff reagent. A colorless, unstable dialdehydecompound is formed and then transformed to the colored final product by restoration of the quinoid chromophoric grouping.
The stain may also be used as an aid in the identification ofCryptococcus neoformans, a pathogenic fungus containing mucin in its capsule. Cryptococcus stained with Mucicarmine Stain.
The eosincomponent stains the parasitenucleus red, while the methylenecomponent stains the cytoplasm blue
CAN BE EASILY DISSEMINATED OR TRANSMITTED FROMPERSON TO PERSON;RESULT IN HIGH MORTALITY RATES AND HAVE THE POTENTIALFOR MAJOR PUBLIC HEALTH IMPACT;MIGHT CAUSE PUBLIC PANIC AND SOCIAL DISRUPTION; ANDREQUIRE SPECIAL ACTION FOR PUBLIC HEALTH PREPAREDNESS. MARBURG MACHUPO]) 3. YERSINIA PESTIS 4. VARIOLA MAJOR 1. BACILLUS ANTHRACIS 5. FRANCISELLA TULARENSIS FILOVIRUSES [E.G., EBOLA, 6. ARENAVIRUSES (E.G., LASSA, 2. CLOSTRIDIUM BOTULINUM TOXIN
Characteristically, the overall vascular system is damaged, and the bodys ability to regulate itself isimpaired. These symptoms are often accompanied byhemorrhage (bleeding); however, the bleeding is itself rarely life-threatening.
-Occurs aprox. 3 weeks after -AKA: Chancaroid - it is a single, red papule that gradually begins to -Haemophilus ducreyi erode -Sexually transmitted -forming a painless, clean infection ulcer with a smooth, raised -Open sores in the border genital region - fluid expressed from the lesion contains the spirochete Treponema pallidum, the causative agent of syphilis.
Persons with latent TB infection do not feel sick and do not have any symptoms. They are infected with M. tuberculosis, but do not have TB disease. Theonly sign of TB infection is a positive reaction to the tuberculin skin test or TB blood test. Persons with latent TB infection are not infectious and cannot spread TB infection to others.
The formerly dormantA person doesn’t know they bacteria multiply and destroy have become infected. At tissue in the lungs. They also this stage of the infection may spread to the rest of the you are not contagious. body via the bloodstream.Macrophages, immune cells Fluid or air may collect that detect and destroy between the lungs and the foreign matter, ingest the lining of the lungs, while TB bacteria and transport tubercles continue to develop them to the lymph nodes in the lung, progressively where they may be destroying lung tissue. inhibited, destroyed, or Coughing of blood or phlegm they may multiply. may occur.
Dry Leprosy - leprosy chiefly affecting the nerves, marked by hyperesthesia succeeded by anaesthesia, and by paralysis, ulceration, and various trophic disturbances, terminating in gangrene and mutilation. Anergic -The more severe form of leprosy, lepromatous leprosy, includes symmetric skin thickening and nodules. This is also called anergic leprosy, because of the unresponsiveness (anergy) of the host immune system. Cooler areas of skin, including the earlobes and feet, aremore severely affected than warmer areas, such as the axilla and groin.
Primary Secondary Tertiary - Chancre - Most contagious - Follows primary infection 3-15 development - Happens 2-8 weeks years after - Enlarged lymph after first development - Pockets of damage occur nodes of chancres within bones, skin, nervous- Bacteria multiplies - Bacteria has spread tissue, heart, and arteries. in blood but very to the blood stream -These areas are called gummas little outward and they are very destructive. evidence
-Infected mosquito transfers Plasmodium to human. -Cells burst within 48-72 hours after Malaria mosquito bite. -Causes chills and Fever -More than 500 infected every year -Infected Tsetse fly transfers Trypanosome brucei. African -50,000-70,000 currently infected today.Trypanosome -First phase; headache, joint pain, and (sleeping fever. Sickness) -Second phase; confusion, day time slumber and night time insomnia.
-Tsetse Fly -Trypanosome brucei -Sleeping sickness African -Suramin, pentamidine and berenil: can cure infection if given before invasion of nervous system -Reduvid Bug -Trypanosome cruzi -Chagas DiseaseAmerican -No effective treatment. -Available drugs only kill extracellular parasites.
Intestinal Hepatic•Asymptomatic passage of •No dysentery cysts •Occurs 8 weeks-1 year •Abdominal pain and •Sweating and pyrexia diarrhea •Dry painful cough•Symptoms fluctuate over •Liver enlargement with weeks-months localized tenderness •Dysentery
Consists of infiltrations and proliferations of lymphocytes and also increased numbers ofastrocytes and microglia.
Kochs postulates are a series of ground rules to determine whether a given organism cancause a given disease. Koch theorized that a pathogen must be: •found in all cases of the disease examined •prepared and maintained in a pure culture•capable of producing the original infection, even after several generations in culture •retrievable from an inoculated animal and cultured again
immune process where particles such as bacteria aretargeted for destruction by an immune cell known as a phagocyte
•Simultaneous infections due to two pathogens. •Example:Co-Infection • Hep C + HIV •Hep B + HIV •Babesiosis + Lyme Disease •Syphilis + HIV •Multiple parasites •Neglected reality •Usually found in theMultiparasitism digestive tract •100-800 million people infected.
(of a disease) prevalentthroughout an entire country,continent, or the whole world; epidemic over a large area
HIV AIDs•Human Immunodeficiency Virus •Acquired Immunodeficiency •Over a Million infected (CDC) Syndrome •Progresses to AIDs •470,000 infected (CDC)•21% of people don’t even know •Retrovirus they are infected •Kills 18,000/year •56,000 infected every year Myths HIV can only infect gay men HIV can only infect IV drug usersMosquitoes don’t spread HIV/AIDs
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